Atherosclerosis最新文献

{"title":"Plasma polyamines levels and post-stroke depression in ischemic stroke patients: A multicenter prospective study","authors":"Yu He ,&nbsp;Xinyue Chang ,&nbsp;Yi Liu ,&nbsp;Jiawen Fei ,&nbsp;Xiaoli Qin ,&nbsp;Beiping Song ,&nbsp;Quan Yu ,&nbsp;Pinni Yang ,&nbsp;Mengyao Shi ,&nbsp;Daoxia Guo ,&nbsp;Yanbo Peng ,&nbsp;Jing Chen ,&nbsp;Aili Wang ,&nbsp;Tan Xu ,&nbsp;Jiang He ,&nbsp;Yonghong Zhang ,&nbsp;Zhengbao Zhu","doi":"10.1016/j.atherosclerosis.2025.119150","DOIUrl":"10.1016/j.atherosclerosis.2025.119150","url":null,"abstract":"<div><h3>Background and aims</h3><div>Polyamines have been suggested to implicated in inflammation, ischemic stroke, and mental disorders, but the associations of polyamines with post-stroke depression (PSD) remain unclear. We aimed to prospectively investigate the associations of plasma putrescine, spermidine and spermine with PSD among ischemic stroke patients in a multicenter cohort study.</div></div><div><h3>Methods</h3><div>We measured plasma putrescine, spermidine and spermine levels at baseline among 635 ischemic stroke patients from a preplanned ancillary study of the CATIS (China Antihypertensive Trial in Acute Ischemic Stroke). The study outcome was depression (Hamilton Depression Rating Scale score ≥8) at 3-month follow-up after ischemic stroke.</div></div><div><h3>Results</h3><div>Plasma putrescine and spermidine were positively associated with the risk of PSD. The adjusted odds ratios of PSD for the highest versus lowest tertile of putrescine and spermidine were 1.77 (95 % CI, 1.13–2.78; <em>p</em>_trend = 0.014) and 1.77 (95 % CI, 1.11–2.82; <em>p</em>_trend = 0.013), respectively. Multivariable-adjusted spline regression analyses showed linear associations of plasma putrescine (<em>p</em> = 0.002 for linearity) and spermidine (<em>p</em> = 0.008 for linearity) with PSD. In addition, plasma putrescine (continuous net reclassification improvement [NRI]: 26.33 %, <em>p</em> = 0.002; integrated discrimination improvement [IDI]: 1.06 %, <em>p</em> = 0.009) and spermidine (continuous NRI: 20.72 %, <em>p</em> = 0.013; IDI: 1.04 %, <em>p</em> = 0.010) could significantly improve the risk reclassification of PSD beyond the established risk factors.</div></div><div><h3>Conclusions</h3><div>High plasma putrescine and spermidine levels were associated with increased risk of PSD among ischemic stroke patients. Our findings suggest that plasma polyamines should be implicated in the pathophysiologic processes of PSD and may be the potential intervention targets for PSD.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119150"},"PeriodicalIF":4.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143549221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global burden and national health inequity of ischemic heart disease attributed to kidney dysfunction from 1990 to 2021: Findings from the global burden of disease study 2021.","authors":"Yue Zhang, Jinyi Wu, Na Wang, Junjie Zhu, Ping Zhang, Xin Wang, Yingying Zhang, Nawi Ng, Lijian Lei","doi":"10.1016/j.atherosclerosis.2025.119140","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.119140","url":null,"abstract":"<p><strong>Background and aims: </strong>To estimate the global disease burden and cross-national inequalities in the distribution of ischemic heart disease attributable to kidney dysfunction (KI-IHD) from 1990 to 2021.</p><p><strong>Methods: </strong>The estimates for age-standardized death rates (ASDR) and age-standardized disability-adjusted life-years rates (ASDAR) of KI-IHD were obtained from the Global Burden of Disease Study (GBD) 2021. Data for gross domestic product (GDP) and GDP growth rates were extracted from World Bank database. The average annual percent change (AAPC) was calculated to analyze temporal trends of ASDR and ASDAR by Joinpoint regression model. Slope index of inequality and concentration index were generated to quantify the cross-national socioeconomic inequality of KI-IHD burden.</p><p><strong>Results: </strong>From 1990 to 2021, the ASDR and ASDAR of KI-IHD has shown downward trend globally; with AAPC values of -1.384 % and -1.204 %. The ASDR and ASDAR of KI-IHD was higher in males than females, with increasing age, the burden gradually increased. The concentration index showed 0.02 (95%CI: 0.02, 0.06) in 1990 and -0.11 (95%CI: 0.15, -0.07) in 2021. The slope index of inequality showed that an excess of 170 ASDR per 100,000 existed between countries with the lowest and the highest SDI in 1990, however, in 2021, the results are reversed, a reduction of 159 per 100,000. GDP growth rate and GDP per capita might be associated with the health inequality of KI-IHD.</p><p><strong>Conclusion: </strong>The burden of KI-IHD has decreased in almost 70 % of countries over the past three decades. Disproportional distribution of health inequalities was concentrated in poor countries.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"119140"},"PeriodicalIF":4.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Claudin 1 dysregulation disrupts coronary microvascular integrity and impairs cardiac function","authors":"Sarmila Nepali ,&nbsp;Min Chen ,&nbsp;Badri Karthikeyan ,&nbsp;Swati D. Sonkawade ,&nbsp;Supriya D. Mahajan ,&nbsp;Joseph Spernyak ,&nbsp;Umesh C. Sharma ,&nbsp;Saraswati Pokharel","doi":"10.1016/j.atherosclerosis.2025.119149","DOIUrl":"10.1016/j.atherosclerosis.2025.119149","url":null,"abstract":"<div><h3>Background and aims</h3><div>Claudin 1 (<em>Cldn1</em>) is a tight junction protein primarily known for its role in epithelial and endothelial barrier function. However, the role of <em>Cldn1</em> in coronary microvascular barrier remain unclear. The aim of this study is to investigate the biological effects of <em>Cldn1</em> dysregulation on coronary vascular permeability, inflammation, fibrosis, and left ventricular function.</div></div><div><h3>Methods</h3><div><em>Cldn1</em> was silenced in human cardiac microvascular endothelial cells (HMVECs) and C57Bl/6 mice using oligonucleotide-based next generation siRNA duplex. Additionally, global transgenic mice with endothelial cell-specific overexpression of <em>Cldn1</em> were created under the regulation of the CD144 (VE-cadherin) promoter. Permeability was assessed using FITC-dextran assay <em>in vitro</em> and Evans blue dye leakage (Mile's assay) in vivo. Cardiac morphology and function were measured by cardiac MRI, and myocardial pathology was analyzed by immunohistochemistry and Transmission Electron Microscopy (TEM). PCR and Western blotting confirmed <em>Cldn1</em> expression changes.</div></div><div><h3>Results</h3><div><em>Cldn1</em> knockdown reduced protein levels by 46% (p = 0.004) and significantly increased endothelial permeability in HMVEC (p = 0.0007). In mice, <em>Cldn1</em> knockdown significantly increased Evans blue dye leakage (p = 0.025), macrophage infiltration (p = 0.018), and interstitial collagen (p = 0.048). TEM confirmed endothelial damage particularly affecting the basement membrane structure. Cardiac MRI showed reduced stroke volume (p = 0.004) and ejection fraction (p = 0.043). <em>Cldn1</em> overexpression reduced vascular permeability (p = 0.002) without altering cardiac function under basal condition.</div></div><div><h3>Conclusion</h3><div><em>Cldn1</em> plays an important role in maintaining coronary microvascular barrier integrity. Its loss leads to increased permeability, inflammation, fibrosis, and impaired cardiac function, while overexpression enhances barrier function without affecting cardiac performance under baseline conditions.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119149"},"PeriodicalIF":4.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transportation noise and the cardiometabolic risk.","authors":"Thomas Münzel, Marin Kuntic, Andreas Daiber, Mette Sørensen","doi":"10.1016/j.atherosclerosis.2025.119148","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.119148","url":null,"abstract":"<p><p>Transportation noise is a widespread and often underestimated environmental pollutant, posing a substantial health risk particularly in urban areas. In contrast to air pollution, the health effects of noise pollution are less extensively documented. Defined as an unwanted and/or harmful sound, noise pollution affects over 20 % of the European Union (EU) population, contributing to an estimated 12,000 premature deaths and 48,000 new cases of ischemic heart disease annually. Recent epidemiological evidence strengthens the link between transportation noise and cardiovascular disease (CVD). A 2024 Umbrella + review with subsequent meta-analyses found that road traffic noise was associated with risk of CVD, more specifically a 4.1 % higher risk for ischemic heart disease, 4.6 % for stroke, and 4.4 % for heart failure per 10 dB(A). Translational and experimental studies have investigated the biological mechanisms behind noise-induced cardiovascular damage, showing that noise impacts stress and sleep pathways. Human studies reveal that nighttime noise impairs vascular function, elevates stress hormone levels, and triggers inflammation and oxidative stress, particularly in individuals with pre-existing CVD. Animal research corroborates these findings, demonstrating that noise exposure leads to endothelial dysfunction, elevated blood pressure, and oxidative stress through mechanisms shared with traditional cardiovascular risk factors. Mitigation strategies are crucial to reducing the health impacts of environmental noise. For road traffic, transitioning to electric vehicles offers minimal noise reduction, necessitating measures such as noise-reducing asphalt, low-noise tyres, and changes in urban infrastructure, whereas for aircraft noise nighttime flight bans and optimized flight paths are important tools for reducing noise exposure. Addressing co-exposure to noise and air pollution is essential for a comprehensive approach to mitigating the environmental burden on cardiovascular health.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"119148"},"PeriodicalIF":4.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The vicious circle of chronic kidney disease and hypertriglyceridemia: What is first, the hen or the egg?","authors":"Tramontano Daniele ,&nbsp;D'Erasmo Laura ,&nbsp;Larouche Miriam ,&nbsp;Brisson Diane ,&nbsp;Lauzière Alex ,&nbsp;Di Costanzo Alessia ,&nbsp;Bini Simone ,&nbsp;Minicocci Ilenia ,&nbsp;Covino Stella ,&nbsp;Baratta Francesco ,&nbsp;Pasquali Marzia ,&nbsp;Cerbelli Bruna ,&nbsp;Gaudet Daniel ,&nbsp;Arca Marcello","doi":"10.1016/j.atherosclerosis.2025.119146","DOIUrl":"10.1016/j.atherosclerosis.2025.119146","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is documented to cause alterations in lipid metabolism, and this was considered a potent driver of increased cardiovascular risk. Among the diverse alteration of lipid traits in CKD, research endeavours have predominantly concentrated on low-density lipoproteins (LDL) in view of the potent pro-atherogenic role of these lipoprotein particles and the demonstration of protective cardiovascular effect of reducing LDL. However, few studies have focused on the metabolism of triglyceride-rich lipoproteins and even fewer on their role in causing kidney damage. Therefore, the comprehensive description of the impact of hypertriglyceridemia (HTG) in CKD pathophysiology remains largely undetermined. This reflects the difficulty of disentangling the independent role of triglycerides (TG) in the complex, bidirectional relationship between TG and kidney disease. Abnormal neutral lipid accumulation in the intrarenal vasculature and renal cells eventually due to HTG may also promote glomerular injury, throughout mechanisms including oxidative stress, mitochondrial dysfunction and proinflammatory responses. While epidemiological and experimental evidence suggests a potential role of TG in kidney damage, the causal mechanisms and their clinical relevance remain unclear, representing a significant area for future investigation. This review aims to highlight the intricate interplay between TG metabolism and kidney disease, shedding light on the mechanisms through which HTG may influence kidney functionality.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119146"},"PeriodicalIF":4.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143579991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune checkpoint inhibitors: Unravelling atherosclerotic cardiovascular risk","authors":"Rhys Gray ,&nbsp;Charlotte Manisty ,&nbsp;Richard Cheng ,&nbsp;Amardeep Dastidar ,&nbsp;Mamas Mamas ,&nbsp;Arjun Ghosh","doi":"10.1016/j.atherosclerosis.2025.119147","DOIUrl":"10.1016/j.atherosclerosis.2025.119147","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119147"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143549218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of bone morphogenetic protein 4 alleviates angiotensin II-induced abdominal aortic aneurysm by reducing inflammation and endothelial-mesenchymal transition","authors":"Yingzheng Weng ,&nbsp;Xihao Wang ,&nbsp;Yimin Tang ,&nbsp;Changqing Du ,&nbsp;Xinyao Li ,&nbsp;Kefu Zhu ,&nbsp;Yizhong Bao ,&nbsp;Wenping Zeng ,&nbsp;Changhong Cai ,&nbsp;Bingbing Jia ,&nbsp;Zhouxin Yang ,&nbsp;Lijiang Tang","doi":"10.1016/j.atherosclerosis.2025.119134","DOIUrl":"10.1016/j.atherosclerosis.2025.119134","url":null,"abstract":"<div><h3>Background and aims</h3><div>Abdominal aortic aneurysm (AAA) is one of the most common fatal macrovascular diseases worldwide which pathogenesis is still not well clarified. In this study, we systematically investigated the alternations of endothelial cell (ECs) functions and phenotypes by single-cell RNA sequencing in angiotensin (Ang) II-induced AAA mice models.</div></div><div><h3>Method and results</h3><div>According to 10 × single-cell sequencing analysis, we revealed that ECs inflammation and endothelial-mesenchymal transition (EndoMT) were involved in the progress of Ang II-induced AAA. Three types of ECs, including <em>Mature ECs</em> (uninjured ECs), <em>EndoMT ECs</em> and <em>Injury &amp; inflammation ECs</em> successively emerged during the progression of AAA. By using pseudotime-trajectory analysis, we speculated bone morphogenetic protein 4 (BMP4) as a candidate gene, participating in Ang II-induced AAA by regulating EndoMT and vascular inflammation. We found that inhibition of BMP4 ameliorated EndoMT and vascular inflammation in Ang II-induced AAA in vivo. In addition, we found that exogenous BMP4 directly promoted the phenotypic transition, inflammation, cell migration and invasion of mouse aortic endothelial cells via PI3K/AKT/mTOR pathways in vitro. Finally, Protein-protein interaction (PPI) analysis and co-immunoprecipitation (Co-IP) revealed that biglycan (BGN) directly combined with BMP4 and promoted the conversion of EndoMT.</div></div><div><h3>Conclusion</h3><div>Our findings firstly revealed a critical role of BMP4 in AAA progression, which promoted disease progression by inducing EndoMT and reprogramming ECs from anti-inflammatory to proinflammatory phenotype.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119134"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143609760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Edgeworthia gardneri (Wall.) Meisn protects against HFD-induced murine atherosclerosis through improving gut microbiota-mediated intestinal barrier integrity","authors":"Le Tang ,&nbsp;Jiangsheng Li ,&nbsp;Mingxuan Luan ,&nbsp;Manman Qin ,&nbsp;Chao Zhong ,&nbsp;Yifeng Zhang ,&nbsp;Yanfei Xie ,&nbsp;Min Shi ,&nbsp;Liang Qiu ,&nbsp;Jun Yu","doi":"10.1016/j.atherosclerosis.2025.119132","DOIUrl":"10.1016/j.atherosclerosis.2025.119132","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Gut microbiota plays a crucial role in the development and progression of atherosclerosis. &lt;em&gt;Edgeworthia gardneri&lt;/em&gt; (Wall.) Meisn, a member of the Thymelaeaceae family and the &lt;em&gt;Edgeworthia&lt;/em&gt; genus, has been previously shown in our studies to attenuate atherogenesis when administered orally as an ethanolic extract (EEEG). However, the interaction between EEEG and gut microbiota, and the mechanism by which gut microbiota exerts anti-atherosclerotic effects, remains unclear.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Aims&lt;/h3&gt;&lt;div&gt;This study aims to determine whether the anti-atherosclerotic properties of EEEG are associated with gut microbiota remodeling.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;Atherosclerosis was induced in &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice using a high-fat diet (HFD). The mice were treated with EEEG or Lactobacillus plantarum for 16 weeks. The composition of gut microbiota was analyzed through 16S rDNA sequencing. To assess whether the anti-atherosclerotic effects of EEEG depend on the gut microbiota, HFD-fed mice were treated with a cocktail of antibiotics or underwent fecal microbiota transplantation (FMT). Simultaneously, plaque areas in the aortic roots and whole aortas of apolipoprotein E deficient (&lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt;) mice were evaluated using oil red O staining and hematoxylin-eosin staining. Serum levels of LPS, fluorescein isothiocyanate-dextran, and expression levels of tight junction proteins were measured to identify the effects of EEEG on gut barrier dysfunction in HFD-fed &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The results revealed that EEEG treatment significantly reduced atherosclerotic lesions by ameliorating lipid accumulation and preserving gut barrier integrity. The protective effects were abrogated by antibiotics administration, concomitant with an increase in gut barrier permeability by decreasing expression of tight junction proteins. The microbial analysis indicated an augmented abundance of &lt;em&gt;Lactobacillus&lt;/em&gt;, &lt;em&gt;Turicibacter&lt;/em&gt;, &lt;em&gt;Faecalibacterium&lt;/em&gt;, &lt;em&gt;Akkermansia&lt;/em&gt;, and &lt;em&gt;Desulfovibrio&lt;/em&gt; following EEEG treatment. Meanwhile, transplantation of fecal microbiota from EEEG-treated mice exerted the anti-atherosclerotic effect in the high-fat diet (HFD)-fed &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; recipient mice, accompanied by improvement of gut barrier integrity through upregulation of tight junction protein expression. Furthermore, exogenous supplementation of &lt;em&gt;Lactobacillus plantarum&lt;/em&gt; mitigated AS in &lt;em&gt;ApoE&lt;/em&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt; mice and improved the gut epithelial barrier function by increasing the expression level of Zo-1.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;These results suggest that the anti-atherosclerotic efficacy of EEEG is attributed to the preservation of gut barrier integrity mediated by gut microbiota. EEEG and its enriched &lt;em&gt;Lactobacillus plantarum&lt;/em&gt; may be promising adjunct","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119132"},"PeriodicalIF":4.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Achieved levels of apolipoprotein B and plaque composition after acute coronary syndromes: Insights from HUYGENS","authors":"Masashi Fujino ,&nbsp;Giuseppe Di Giovanni ,&nbsp;Julie Butters Bhsc ,&nbsp;Yu Kataoka ,&nbsp;Thomas Hucko ,&nbsp;Adam J. Nelson ,&nbsp;Steven E. Nissen ,&nbsp;Peter J. Psaltis ,&nbsp;Stephen J. Nicholls","doi":"10.1016/j.atherosclerosis.2025.119145","DOIUrl":"10.1016/j.atherosclerosis.2025.119145","url":null,"abstract":"<div><h3>Background and aims</h3><div>Addition of the PCSK9 inhibitor, evolocumab, to statin therapy promoted coronary plaque stabilization after an acute coronary syndrome. While apolipoprotein B (ApoB) has been proposed as a goal for lipid-lowering therapy in the prevention of cardiovascular disease, its association with plaque stability has not been studied.</div></div><div><h3>Methods</h3><div>The High-Resolution Assessment of Coronary Plaques in a Global Evolocumab Randomized Study (HUYGENS) used serial optical coherence tomography to assess coronary plaque phenotypes in patients with non-ST elevation myocardial infarction treated with evolocumab plus statin or placebo plus statin for 52 weeks. Changes in plaque composition were studied in patients according to achievement of a goal ApoB level &lt;65 mg/dL.</div></div><div><h3>Results</h3><div>Of 112 patients, 67 (59.8 %) achieved the ApoB goal and had lower ApoB values at follow-up compared with those not at goal (37.1 ± 15.0 vs 92.7 ± 19.4 mg/dL, P &lt; 0.001). Patients achieving the ApoB goal demonstrated a greater increase in minimum fibrous cap thickness (+44.6 ± 36.0 vs +24.9 ± 38.1 μm, P = 0.007) and a more pronounced decrease in lipid arc (−57.8 ± 52.8 vs −27.0 ± 59.2°, P = 0.005) at follow-up, compared with those who did not achieve the ApoB goal. At follow-up, thin-cap fibroatheroma (TCFA) was less prevalent among patients achieving the ApoB goal compared with those not at goal (9.0 vs. 40.0 %, P &lt; 0.001). Multivariate analysis demonstrated that achieving an ApoB &lt;65 mg/dL at follow-up independently associated with the absence of TCFA at follow-up (P = 0.004).</div></div><div><h3>Conclusions</h3><div>Lower achieved ApoB levels associated with evidence of greater plaque stabilization even after controlling for low-density lipoprotein cholesterol levels. This highlights the importance of optimizing ApoB levels for the reduction of cardiovascular risk.</div></div><div><h3>Clinicaltrialsgov identifier</h3><div>NCT03570697.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119145"},"PeriodicalIF":4.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term body mass index trajectories and the risk of type 2 diabetes mellitus and atherosclerotic cardiovascular disease using healthcare data from UK Biobank participants","authors":"Anja Krüger ,&nbsp;Ko Willems van Dijk ,&nbsp;Diana van Heemst ,&nbsp;Raymond Noordam","doi":"10.1016/j.atherosclerosis.2025.119135","DOIUrl":"10.1016/j.atherosclerosis.2025.119135","url":null,"abstract":"<div><h3>Background and aims</h3><div>Most epidemiological studies ignore long-term burden, gain and variability in body weight in assessing cardiometabolic disease risk. We investigated the associations of body mass index (BMI) trajectories measured by general practitioners with incident type 2 diabetes (T2D) and coronary artery disease (CAD).</div></div><div><h3>Methods</h3><div>We used electronic healthcare data from 111,615 European-ancestry participants from UK Biobank (57.1 (SD 7.8) years, 59.6 % women) with at least three BMI measurements (median trajectory period: 14.9 [interquartile range 9.5, 20.1] years). We calculated six variables capturing different long-term aspects, including i.e. burden (long-term average, area under the curve), gain (slope) and variability (standard deviation, average of the [absolute] consecutive BMI differences). The variables were used in principal component (PC) analyses and k-means clustering. Newly-derived dimensions and subgroups were used as exposures in cox-proportional hazard models.</div></div><div><h3>Results</h3><div>The BMI-trajectory indices were captured in two PCs reflecting BMI burden and BMI gain. The BMI-burden PC associated with higher T2D (hazard ratio [95 % confidence interval] per SD higher PC: 1.57 [1.55,1.60]) and CAD (1.17 [1.15,1.19]) risks, while weak or no associations were observed with the BMI-gain PC (T2D: 1.03 [1.01,1.05]; CAD: 1.01 [0.98,1.03]). Participants with the highest BMI burden, compared to those with lowest BMI burden without significant gain, had highest T2D (6.96 [6.41,7.55]) and CAD (1.57 [1.45,1.69]) risks. Both methods to capture BMI burden, gain and variability showed superior model fit compared to a single baseline BMI assessment.</div></div><div><h3>Conclusions</h3><div>Long-term high BMI burden, irrespective of BMI gain, was a risk factor for cardiometabolic disease.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119135"},"PeriodicalIF":4.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}